A Biomarker-Enhanced Model for Prediction of Acute Kidney Injury and Cardiovascular Risk Following Angiographic Procedures: CASABLANCA AKI Prediction Substudy

Abstract

BACKGROUND: The 2020 Acute Disease Quality Initiative Consensus provided recommendations on novel acute kidney injury biomarkers. In this study, we sought to assess the added value of novel kidney biomarkers to a clinical score in the CASABLANCA (Catheter Sampled Blood Archive in Cardiovascular Diseases) study. METHODS AND RESULTS: We evaluated individuals undergoing coronary and/or peripheral angiography and added 4 candidate biomarkers for acute kidney injury (kidney injury molecule-1, interleukin-18, osteopontin, and cystatin C) to a previously described contrast-associated acute kidney injury (CA-AKI) risk score. Participants were categorized into integer score groups based on the risk assigned by the biomarker-enhanced CA-AKI model. Risk for incident cardiorenal outcomes during a median 3.7 years of follow-up was assessed. Of 1114 participants studied, 55 (4.94%) developed CA-AKI. In adjusted models, neither kidney injury molecule-1 nor interleukin-18 improved discrimination for CA-AKI; addition of osteopontin and cystatin C to the CA-AKI clinical model significantly increased the c-statistic from 0.69 to 0.73 (P for change <0.001) and resulted in a Net Reclassification Index of 59.4. Considering those with the lowest CA-AKI integer score as a reference, the intermediate, high-risk, and very-high-risk groups were associated with adverse cardiorenal outcomes. The corresponding hazard ratios of the very-high-risk group were 3.39 (95% CI, 2.14–5.38) for nonprocedural acute kidney injury, 5.58 (95% CI, 3.23–9.63) for incident chronic kidney disease, 6.21 (95% CI, 3.67–10.47) for myocardial infarction, and 8.94 (95% CI, 4.83–16.53) for all-cause mortality. CONCLUSIONS: A biomarker-enhanced risk model significantly improves the prediction of CA-AKI beyond clinical variables alone and may stratify the risk of future cardiorenal outcomes.